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Quarter 4 > Pharm Exam I > Flashcards

Pharm Exam I Flashcards

1
Q

aka Cranial-sacral

A

Parasympathetic

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2
Q

aka Thoraco-lumbar

A

Sympathetic

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3
Q

Effector and Function of alpha-1

A

smooth muscles and sphincters

contraction (constriction)

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4
Q

Effector and Function of alpha-2

A

Nerve endings

decrease transmitter release

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5
Q

Effector and Function of Beta-1

A

cardiac muscle and kidney

increase HR and contractility, increase renin

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6
Q

Effector and Function of Beta-2

A

smooth muscle (bronchi), liver, and skeletal muscle

relax smooth muscle, gluconeogenesis, increase K+

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7
Q

Effector and Function of Beta-3

A

Adipose

increase lipolysis

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8
Q

Effector and Function of DA-1

A

Smooth muscle (renal), mesenteric, and cardiac

relax renal SM

  • higher doses activates B1 and A1 receptors
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9
Q

Pathway of catecholamine biosynthesis

A

Phenylalanine

Tyrosine

Dopa

Dopamine

Norepinephrine

Epinephrine

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10
Q

All catecholamines are rapidly inactivated by ___ and ___

A

MAO ro COMT

  • Monoamine oxidase
  • catechol-O-methyltransferase
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11
Q

What drugs should not be given with MAO inhibitors?

A
  • antihistamines
  • antihypertensives
  • barbituates
  • CNS depressants
  • OTC cold meds
  • tricyclic antidepressants
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12
Q

3 common MAO inhibitors

A

Nardil, Parnate, and Marplan

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13
Q

(3) naturally occuring catecholamines

A

Epinephrine, Norepinephrine, and Dopamine

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14
Q

(2) non-catecholamine sympathomimetics

A

Ephedrine and Phenylephrine

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15
Q

(2) Synthetic catecholamines

A

Isoproterenol and Dobutamine

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16
Q

(3) selective Beta-2 agonists

A

albuterol, metaproterenol, and terbutaline

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17
Q

(1) cardiac glycoside

A

digoxin

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18
Q

(2) phosphodiesterase inhibitor

A

Amrinone and Milrinone

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19
Q

Epinephrine doses for Cardiac arrest

A

0.1 ml/kg of 1:1000 ETT

or

0.1 ml/kg of 1:10,000 IV

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20
Q

Epinephrine dose for Status Asthmaticus

A

0.01 mg/kg of 1:1000 sq

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21
Q

Epinephrine storage and release

A

adrenal medulla

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22
Q

Administration of Epinephrine

A

oral administration is not effective

  • Must use sub-q, IV, IM, IO, or via ETT
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23
Q

Why does Epi not affect the brain?

A

poorly lipid soluble

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24
Q

Cardiovascular effects of Epineprhine

A

increases HR by accelerating rate of phase 4 depolarization

  • increase risk of dysrhythmias
  • chronic Epi reduces plasma volume
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25
Q

Respiratory effects of Epinephrine

A

Bronchodilator

  • unless patient is BB, then it causes bronchoconstriction from stimulating bronchial alpha receptors
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26
Q

Other effects of Epinephrine

A
  • most significant effect on metabolism
  • may activate Na+-K+ pump and transfer K+ into cells
  • mydriasis
  • accelerates coagulation
    • increases total leukocytes
    • increases factor V
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27
Q

Which catecholamines have no effect on Alpha?

A

Isoproterenol and Dobutamine

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28
Q

Which catecholamines have the greatest effect on Alpha?

A

Norepinephrine and Phenylephrine

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29
Q

Which catecholamine has no effect on Beta-1

A

Phenylephrine

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30
Q

Which catecholamines have the most effect on Beta-1

A

isoproterenol and dobutamine

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31
Q

Which catecholamine has the most effect on Beta-2

A

Isoproterenol

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32
Q

Which catecholamine is indirect and direct

A

Ephedrine

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33
Q

Which catecholamines have a negative impact on CO and HR?

A

Norepinephrine and Phenylephrine

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34
Q

Which catecholamine has a large negative effect on peripheral vascular resistance?

A

Isoproterenol

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35
Q

Which two catecholamines cause the greatest increase in peripheral vascular resistance and MAP?

A

Norepinephrine and Phenylephrine

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36
Q

Synthesis and storage of Norepinephrine

A

postganglionic sympathetic nerve endings

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37
Q

Norepinephrine in treatment of refractory hypotension

A

continuous infusion (2-16 ug/min) in severe sepsis

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38
Q

Side effects of Norepinephrine

A
  • avoid in right ventricular failure
    • increase venous return to heart and increases the pulmonary artery pressure
  • may decrease CO and increase work of left ventricle
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39
Q

Low dose Dopamine

A

(0.5 - 3 mcg/kg/min)

  • primarily stimulates D1 and D2
  • increases splanchnic and renal flow
  • diuresis
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40
Q

negative side effects of Dopamine

A
  • tachycardia in high doses
  • increased pulmonary vascular resistance
    • not good for right heart failure
  • does NOT provide renal protection
    • may cause harm in patients with renal disease by redistributing blood flow in the kidney
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41
Q

Clinical use for Dopamine

A

increase cardiac output in patients with decreased contractility, low systemic blood pressure and low urine output

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42
Q

Cardiovascular effects of Dopamine

A

higher risk of developing sinus tachycardia and ventricular arrhythmias

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43
Q

Isoproterenol Overview

A
  • most potent sympathomimetic
  • no alpha effects
  • rapidly metabolized by COMT
    • neees a continuous infusion
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44
Q

Clinical uses of Isoproterenol

A

increases the HR in patients with heart block

  • useful before insertion of pacemaker
  • useful in pulmonary hypertension and right ventricular dysfunction
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45
Q

Adverse effects of Isoproterenol

A

vasodilation and decreased blood pressure

  • can lead to myocardial ischemia
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46
Q

Dobutamine overview

A

Potent Beta-1, weak Beta-2 and increasing effect on Alpha at higher doses

  • racemix mixture
  • decreases pulmonary vascular resistance
    • inhibits HPV
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47
Q

Clnical uses for Dobutamine

A

can improve cardiac output in patients with CHF and wean patients off cardiopulmonary bypass

  • stress testing
  • pulmonary hypertension
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48
Q

Ephedrine Overview

A

indirect alpha and beta agonist

  • resistant to MAO in the GI tract
    • drug can be absored after oral administration
  • does not produce hyperglycemia
  • CNS stimulation occurs
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49
Q

Clincial use for Ephedrine

A

increases systemic blood pressure

  • tachyphylaxis occus
  • no longer drug of choice for deliveries
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50
Q

Cardiovascular effects of Ephedrine

A
  • less potent in raising BP and lasts approximately 10x longer than epinephrine
  • increases systolic and diastolic BP, HR, and CO
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51
Q

Tachyphylaxis

A

second dose of a drug is less intense than the first

  • occurs with many sympathomimetics
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52
Q

Phenylephrine Overview

A

synthetic noncatecholamine that mimics the effects of Norepineprhine, but is less potent and longer lasting

  • increases venoconstriction
  • must be double diluted
  • increases coronary perfusion without chronotropic side effects
    • good for CAD and aortic stenosis
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53
Q

Cardiovascular effects of Phenylephrine

A

peripheral vasoconstriction and increases systemic blood pressure, while decreasing CO

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54
Q

Phenylephrine Toxicity Treatment

A
  • direct acting vasodilator (alpha antagonist)
    • Ex: Phentolamine
  • beta blockers are contraindicated
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55
Q

Digoxin Overview

A

Used for supraventricular tachydysrhythmias (paroxysmal atrial tachycardia, a-fib, and a-flutter)

  • decrease conduction through the AV node
  • 10-30min IV onset
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56
Q

Narrow Therapeutic range for Digoxin

A
  • Causes
    • renal dysfunction
    • hypoxemia
    • hypokalemia
    • hypercalcemia
    • hypermagnesemia
  • Diagnosis
    • plasma concentration
    • anorexia, nausea, vomiting
    • EKG
      • atrial and ventricular arrhythmias
      • long PR or heart block
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57
Q

Digoxin Toxicity Treatment

A
  • correct causes
    • hypokalemia
    • hypoxemia
  • Phenytoin, lidocaine, or atropine
    • treat cardiac dysrhythmias
  • temporary pacemaker
    • if complete heart block
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58
Q

Contraindications for Digoxin

A
  • Hypertrophic obstructive cardiomypathy (HOCM)
    • IHSS
    • ASH
  • increased contractility may exacerbate outflow obstruction
  • Wolff-Parkinson-White syndrome
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59
Q

IHSS

A

idiopathic hypertrophic subaortic stenosis

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60
Q

ASH

A

asymmetric septal hypertrophy

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61
Q

WPW EKG

A

short PR interval with delta wave

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62
Q

Selective Phosphodiesterase Inhibitors

A
  • increase cAMP in myocardial and vascular
  • increased inward Ca2+ current
    • increases contractility
    • vasodilation
  • effective in BB patients
  • enhance actions of catecholamines
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63
Q

Effects of Phosphodiesterase Inhibitors

A
  • decrease SVR, PVR, and CVP
  • increase contractility (inotropy)
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64
Q

Uses for Calcium

A
  • after massive transfusion
  • CP bypass
  • following parathyroidectomy
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65
Q

How should calcium chloride be given?

A

through a central line

  • always aspirate first
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66
Q

(2) Alpha Antagonists

A

Phentolamine and Phenoxybenzamine

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67
Q

(4) Alpha-1 antagonists

A
  • Prazosin (minipress)
  • Doxazosin (cardura)
  • Terazosin (hytrin)
  • Tamulosin (flomax)
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68
Q

(2) Alpha-2 Agonists

A

Clonidine and Dexmedotomidine

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69
Q

(2) Combinded Alpha and Beta Antagonists

A

Labetolol and Carvedilol

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70
Q

(6) Calcium Channel Blockers

A
  • Amlodipine
  • Diltiazem
  • Nicardipine
  • Nifedipine
  • Nimodipine
  • Verapamil
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71
Q

Primary mechanism of Norepinephrine termination

A

reuptake

72
Q

preganglionic neurtransmitter of the parasympathetic system

A

acetylcholine

73
Q

preganglionic neurotransmitter of the sympathetic system

A

acetylcholine

74
Q

postganglionic neurotransmitter of the sympathetic system

A

Norepinephrine

75
Q

Sensitivity for Alpha and Beta receptors

A

Alpha-1 NE > Epi

Alpha-2 NE > Epi

Beta-1 Epi >= NE

Beta-2 Epi > NE

76
Q

locations of Alpha-1 receptors

A
  • vascular smooth muscle
  • heart
  • GI smooth muscle
  • liver
77
Q

locations of Alpha-2 receptors

A
  • CNS
  • nerve endings
  • vascular smooth muscle
  • platelets
  • pancreas
78
Q

locations of Beta-1 receptors

A

heart and kidney

79
Q

locations of Beta-2 receptors

A

smooth muscle and skeletal muscle

80
Q

Alpha-1 agonism

A

smooth muscle contraction

81
Q

Alpha-2 agonism

A

inhibition of NE release at the presynaptic terminal

82
Q

Alpha blockers

A

prevent the effects of catecholamines and sympathomimetics on the heart and vasculature

  • Side effects:
    • orthostatic hypotension
    • reflex tachycardia
    • impotence
83
Q

Phentoloamine

(regitine)

A

non-selective alpha antagonist

  • used in hypertensive emergencies
    • pheochromocytoma
    • hyperreflexia
  • Alpha 1 and 2
84
Q

Phenoxybenzamine

(dibenzyline)

A

non-reversible and non-selective alpha antagonist

  • administered orally
  • give 10-14 days before pheochromocytoma removal
  • may cause orthostatic hypotension
  • may be useful in Raynaud’s disease
85
Q

Symptoms of Pheochromocytoma

A
  • sporadic elevations in blood pressure
  • diaphoresis
  • headaches
  • palpitations
  • anxiety/panic attacks
  • malignant hypertension
86
Q

Pre-op preparation for Pheochromocytoma removal

A
  • Outpatient
    • alpha blockade (phenoxybenzamine)
    • titrate alpha blocker
    • add CCB if needed
    • add BB for tachycardia
  • Inpatient
    • fluid replacement
87
Q

In a patient treated with propranolol and phenoxybenzamine prior to resection of a solitary pheochromocytoma, would you expect postoperative hypotension or hypertension?

A

Hypotension

  • hypovolemia
  • residual beta block
  • adrenal insufficiency
  • residual alpha block
88
Q

Doxazosin

(Cardura)

A

used for hypertension and BPH

  • relaxes prostatic and vascular smooth muscle
  • Alpha-1
89
Q

Prazosin

(minipress)

A

used for hypertension and CHF

  • dilates arterioles and veins
  • Alpha-1
90
Q

Terazosin

(Hytrin)

A

treats BPH

  • Alpha-1
91
Q

Tamulosin

(Flomax)

A

treats BPH and may cause orthostatic hypotension

  • Alpha-1A
92
Q

Alpha-2 Receptor Agonists

A
  • act like Alpha-1 antagonists
  • mostly in CNS
  • reduce norepinephrine release by a negative feedback system
93
Q

Clonidine

A
  • used to treat hypertension
  • decrease HR and BP
  • central sedative effect
  • added to regional anesthetics
94
Q

Dexmedetomidine

A
  • sedative and analgesic
  • metabolized in liver
    • liver impairment dramatically impairs plasma level and duration
  • withdrawal may occur
95
Q

Response of Beta-1

A

increase heart rate and contractility

96
Q

Response of Beta-2

A

bronchial and vascular SM relaxation

97
Q

How much beta receptors in the heart are Beta-1?

A

75%

98
Q

Treatment of Acute Coronary Syndrome

A
  • treat with BB for acute MI
    • unless severe bradycardia, unstable LV failure, or AV block
99
Q

ST depression vs elevation

A

Depression signifies a reversible ischemic event that is happening currently

Elevation signifies damage has already been done

100
Q

Perioperative BB

A
  • used in high risk surgeries
    • thoracic, intraperitoneal, vascular
  • maintain 65-80 bpm
  • Atenolol or Metoprolol
  • POISE Study
    • prevents nonfatal MI, but increases risk of stroke, death, hypotension, and bradycardia
101
Q

Treatment drugs for Intraoperative MI

A
  • Esmolol
  • Metoprolol
  • Atenolol
  • Propanolol
102
Q

Management of CHF

A
  • improved survival with oral:
    • Metoprolol
    • Carvedilol
    • Bisoprolol
103
Q

Treatment for BB Toxicity

A
  • Atropine
  • Isoproterenol
  • Dobutamine
  • Glucagon
  • Calcium Chloride

Also external or transvenous pacing and/or dialysis

104
Q

Contraindication of nonselevtice B-blockers

A

bronchial asthma

105
Q

Beta-1 Blockers and Diabetics

A

can impair recovery of hypoglycemia and mask symptoms of hyperglycemia

106
Q

Which BB does not cross the placenta?

A

Esmolol

107
Q

Contraindications to Beta Blockers

A
  • Dysrhythmias
    • first degree heart block
    • second degree Type II
    • third degree
    • sinus arrest
    • sick sinus syndrome
  • hypovolemia with compensatory tachycardia
  • COPD (relative)
  • unopposed alpha stimulation
    • cocaine abuse
    • pheochromocytoma therapy
108
Q

Propranolol

(Inderal, Ipran)

A
  • Beta blocker
  • pure antagonist
    • lacks intrinsic sympathomimetic activity
  • highly protein bound
    • heparin will decrease bound drug
  • increased local anesthetic toxicity
    • especially Bupivicaine
      *
109
Q

Esmolol

(Brevibloc)

A
  • quick onset and offset
  • selective B1-blocker
    • caution in treatment of excess sypathetic outflow
    • beta blockade results in unopposed alpha activity
110
Q

Metoprolol

(lopressor)

A
  • beta-1
    • large doses become non-selective
  • oral and IV
111
Q

Timolol

A

Beta-1 and Beta-2 used for glaucoma

  • systemic absorption can cause bradycardia and increased airway resistance
112
Q

Labetalol

(Trandate)

A

Beta blocker and Alpha-1

  • Uses
    • hypertension and pregnancy induced
    • intuabtion and emergence
    • controlled hypotension
113
Q

Carvedilol

(coreg)

A

beta and alpha-1 antagonist

  • mild to moderate CHF
  • hypertension
114
Q

(2) CCB selective for AV node

A

benzothiazepines and Phenylalklamines

115
Q

CCB selective for arteriolar beds

A

Dihydropyridines

116
Q

Effects of CCB

A
  • slow heart rate
    • decrease speed of conduction through SA and AV node
  • reduce cardiac contractility
  • relax vascular smooth muscle
117
Q

Uses for CCB

A
  • Coronary artery spasm
  • chronic and stable angina
  • Supraventricular tachycardia (SVT)
118
Q

Prinzmetals Angina

A

coronary artery spasms

119
Q

Phenylalkylamine

(verapamil)

A
  • Used in SVT, a-fib, and a-flutter
  • slows conduction through AV node
  • negative chronotropic effect on SA node
  • negative inotrope
  • vasodilates coronary and systemic arteries

May precipitate ventricular dysrhythmias in patients with WPW syndrome

120
Q

(5) Dihydropyridines

A
  • Nifedipine
  • nicardipine
  • Nimodipine
  • Amlodipine
  • Felodipine
121
Q

Which CCBs increases or has no change to heart rate?

A

Nifedipine and Nicardipine

122
Q

Which CCB has moderate SA depression?

A

Verapamil

123
Q

Which CCBs have AV node conduction?

A

Verapamil > Diltizaem

124
Q

Which CCB has the greatest coronary artery dilation?

A

Nicardipine

125
Q

Cytoprotection

A

process by which chemical compounds provide protection to cells against harmful agents

126
Q

Pacemaker Potential

A

Na influx, Ca influx, rapid Ca influx, K outflux

127
Q

Phases of Cardiac Action Potential

A
  • 0 - Na enters the cell (depolarizaton)
  • 1 - close Na, open K
  • 2 - Ca enters the cell (contraction)
  • 3 - K exits the cell (repolarization)
128
Q

Purkinje Fiber vs. SA node

A
  • If is main source in Purkinje
    • If and ICa in SA node
  • Purkinje lower resting potential
  • Purkinje steeper spontaneous depolarization slope
    *
129
Q

(2) basic mechanisms of arrhythmias

A

reentry and enchanced automaticity

130
Q

Factors that facilitate arrhythmias

A
  • hypoxemia
  • electrolye imbalance
  • myocardial ischemia
  • atrial or ventricular enlargement
  • alterted sympathetic nervous activity
  • bradycardia
  • certain drugs
131
Q

Bradycardia predisposes what type of arrhythmias?

A

ventricular

132
Q

If arrhythmias occur from volatile agents, they most likely arose from which mechanism?

A

re-entry

133
Q

ECG and membrane potential of ventricular cell

A
134
Q

Class IA antiarrhythmic

(example)

A

Procainamide

135
Q

Class 1B antiarrhythmic

(example)

A

lidocaine

136
Q

Class 1C antiarrhythmic

(2 examples)

A

flecainide and propafenone

137
Q

Class II antiarrhythmic

(example)

A

esmolol

138
Q

Class III antiarrhythmic

(2 examples)

A

amiodarone and sotalol

139
Q

Class IV antiarrhythmic

(2 examples)

A

verapamil and diltiazem

140
Q

Class 1 agents

A

inhibit fast sodium channels during depolarization

(phase 0)

  • decreases in depolarization rate and conduction velocity
141
Q

Class 1A effects

A
  • Sodium channel blockade
    • length action potential
    • lengthen refractory period
  • Potassium channel blockade
    • prolonged repolarization
142
Q

Side effects of Quinidine

A
  • low therapeutic ratio
  • allergic reaction
  • accentuates effects of NMB
143
Q

Procainamide

A

treats ventricular tachyarrhythmias

  • class 1A
  • drug of choice for stable V-tach
144
Q

Class 1B antiarrhythmics

A
  • less powerful than sodium blockers
  • shorten the action potential duration and refractory period
    • opposite of Class 1A
145
Q

Side effects of phenytoin

A
  • hypotension
  • bone marrow suppression
    • thrombocytopenia
146
Q

Class 1C antiarrhythmics

A
  • potent sodium blockers
    • decrease rate of phase 0 depolarization
    • decrease speed of conduction
  • little effect on duration of AP and refractory period
    • inhomogeneity
    • proarrhythmic effect
  • given if failed conversion from A-fib
    • not the first choice
147
Q

Class II antiarrhythmics

A
  • Beta Antagonists
  • decrease rate of spontaneous (phase 4) depolarization
    • decrease ANS activity
    • supression of ventricular activity during MI
  • treats arrhythmias due to SNS activity
    • a-fib and a-flutter
148
Q

Effective beta blockade

A

55-60 bpm

149
Q

side effects of beta blockers

A
  • bradycardia
  • hypotension
  • myocardial depression
  • bronchospasm
150
Q

Class III antiarrhythmics

A
  • blocks potassium channels
    • prolongation of depolarization, action potential duration, and refractory period
151
Q

Pulmonary toxicity of Amiodarone

A
  • pneumonitis
  • high FiO2 may accelerate reactions
    • restrict inspired O2 to lowest necessary
  • can be slow or acute
152
Q

Amiodarone side effects

A
  • inhibits p450 enzymes
    • increases plasma concentrations of digoxin, procainamide, quinidine, and warfarin
    • decreases digoxin
    • increasesd effect of Warfarin because amiodarone depresses Vitamin K
  • thyroid dysfunction
    • has a high iodine content
  • exhibits class I, class II, and class IV
153
Q

Sotalol side effects

A
  • tosade de pointes
  • bradycardia
  • not recommended in patients with asthma, ventricular dysfunction, and prolonged QTc intervals
154
Q

Class IV antiarrhythmics

A
  • inhibits inward slow Ca currents
    • decreased rate of sponatenous phase 4 depolarization
  • controls the ventricular rate in a-fib and a-flutter
155
Q

Half life of Adenosine

A

10 seconds

156
Q

Adenosine

A
  • slows conduction through AV node
  • temporarily stops heart
  • used to treat SVT
157
Q

Proarrhythmic effects of antiarrhythmics

A
  • torsades de pointes
  • ventricular tachycardia
  • wide complex ventricular rhythm
158
Q

Which antiarrhythmic is recommended prophylactically (oral)?

A

Amiodarone

159
Q

Which class of antiarrhythmics experienced a higher incidence of sudden cardiac arrest?

A

Class IC

(flecainide and propafenone)

160
Q

automatic implantable cardiac defibrilator (AICD)

A

placed if EF less than 30% or intractable arrhythmias

161
Q
A

sustained V-tach

treat with amiodarone, lidocaine, or shock

162
Q
A

Torsade’s de Pointes

treat with magnesium and shock

163
Q

patients with unstable tachycardia should be treated immediately with _____

A

synchronized cardioversion

164
Q

Amiodarone

A
  • Beta Antagonist
  • contains iodine
  • dilates coronary arteries and increase coronary blood flow
165
Q

Which Class of Antiarrhythmics decrease phase 0 (depolarization rate)?

A

1A and 1C

166
Q

Which class of Antiarrhythmic drugs do not decrease the conduction velocity?

A

1B and IV

167
Q

Which class of Antiarrhythmic drugs decrease the refarctory period?

A

1B and II

168
Q

Which class of Antiarrhythmic drugs increase the QRS duration?

A

1A, 1C, and III

169
Q

Which class of Antiarrhythmic drug has no effect on automaticity?

A

Class IV

170
Q

Which class of Antiarrhythmic drugs inhibit slow calcium channels?

A

Class IV

171
Q

Which class of Antiarrhythmic drugs inhibit potassium channels?

A

Class III

172
Q

Which class of Antiarrhythmic drugs inhibit fast sodium channels?

A

Class I

173
Q

Pacemaker Potential

A
174
Q
A

Norepinephrine increases the slope of repolarization therefore increasing the heart rate

175
Q
A

Quarter 4 (15 decks)

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